ArticleScientific reports2025
Identification of biomarkers associated with mitophagy in bladder cancer.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Mitophagy in bladder cancer: a double-edged sword in tumor progression and therapy.Journal of translational medicine · 2026Review
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Authors and funding
8 authors.
Funding
Abstract
Bladder cancer (BLCA) is the most prevalent malignant tumor of the urinary system. Mitophagy is a selective form of autophagy that occurs within the mitochondria. The goal of this study was to determine mitophagy-related biomarkers associated with BLCA and to explore their underlying molecular mechanisms. CTSK, MTERF3, SRC, and CSNK2B were identified as biomarkers. A risk model classified BLCA patients into high-risk group (HRG) and low-risk group (LRG), with HRG patients exhibiting lower survival probabilities. The "chemical carcinogenesis-DNA adducts" and "cytokine-cytokine receptor interaction" signaling pathway were closely associated with HRG and LRG. TP53 had the highest mutation frequencies in the HRG and LRG, respectively. The two groups exhibited significant differences in 14 immune cells, including M2 macrophages. CTSK exhibited the strongest correlation with the naive B cells. A total of 135 drugs differed in sensitivity between HRG and LRG, including KU.55933. The identified regulatory network included ADAMTSL4-AS1-hsa-miR-149-5p-SRC. Expression analysis showed that CTSK was significantly downregulated in the BLCA group, while MTERF3, SRC, and CSNK2B were significantly upregulated. In conclusion, CTSK, MTERF3, SRC, and CSNK2B laid the foundation for targeted therapy in the treatment of BLCA.
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